RCSI Staphylococci Past Paper PDF

Leading the world to better health Staphylococci Dr Aoife Kearney (PhD) Clinical Lecturer 6th November 2023  RCSI Royal College of Surgeons in Ireland Coláiste Ríoga na Máinleá in...

Leading the world to better health Staphylococci Dr Aoife Kearney (PhD) Clinical Lecturer 6th November 2023  RCSI Royal College of Surgeons in Ireland Coláiste Ríoga na Máinleá in Click to edit master title style Éirinn Session ID: BMFML1 Staphylococci R C S I L E A D I N G T H E W O R L D T O B E T T E R H E A LT H Class: Year 1 Course: Undergraduate Medicine Lecturer: Dr Aoife Kearney PhD Date: Presenter Name Title, Department, RCSI 6th November 2024 LEARNING OUTCOMES By the end of the lecture you will be able to……… 1. Outline the basic laboratory features of staphylococci 2. Describe the pathogenesis of infections caused by clinically important staphylococci 3. Recognise and describe the clinical features and complications of infections caused by clinically important staphylococci 4. Outline the laboratory diagnosis of infections caused by clinically important staphylococci 5. Choose the appropriate antimicrobial agents to treat infections caused by clinically important staphylococci 6. Discuss the epidemiology of clinically important staphylococci 7. Use the appropriate measures to prevent the acquisition and spread of infections caused by clinically important staphylococci STAPHYLOCOCCI: BASIC FEATURES Staphylococcus is a genus of Gram-positive bacteria They appear spherical (cocci) and form in clumps / clusters They are facultative anaerobes Traditionally divided into 2 groups based on their ability to clot blood plasma (the coagulase reaction / test) 1. Coagulase-positive staphylococci (S. aureus) Can colonise nasal passages and other moist skin areas (ex. axilla, groin) 2. Coagulase-negative staphylococci (>30 other species) Common human skin commensals (ex. S. epidermidis)  COAGULASE TEST A laboratory test used to differentiate S. aureus (coagulase +ve) from other staphylococci (negative) Coagulase is an enzyme that can cause blood clot formation (converting fibrinogen to fibrin) – Allows bacteria to coat its surface with fibrin & possibly resist phagocytosis  CATALASE TEST Used to differentiate staphylococci from streptococci (also a Gram-positive coccus) Staphylococci = CATALASE + Presence of catalase (an enzyme) is determined by the ability of the bacteria to reduce hydrogen peroxide into water and oxygen – this results in the production of bubbles  CLINICAL CASE 1 A 19 year old male presents to your general practice with a painful, red lump on his neck WHICH ONE OF THE FOLLOWING BESTS DESCRIBES THIS LUMP? A. Acne B. Blister C. Carbuncle D. Cold sore E. Furuncle WHICH ONE OF THE FOLLOWING STAPHYLOCOCCI IS THE MOST LIKELY CAUSATIVE PATHOGEN? A.Staphylococcus aureus B.Staphylococcus capitis C.Staphylococcus epidermidis D.Staphylococcus hominis E.Staphylococcus saprophyticus IS THE INFECTION EXOGENOUS OR ENDOGENOUS? A.Exogenous B.Endogenous DOES THIS INFECTION REQUIRE ANY FURTHER MANAGEMENT? A.Yes B.No  1. Staphylococcus aureus Found in moist skin folds, mucosal surfaces, nasopharynx – 20 – 40% healthy humans colonised – Increased if: Diabetes mellitus Injecting drug use Where a foreign body/implant is present Distinguished as being methicillin-sensitive (MSSA) or resistant (MRSA) – Resistance to usual treatment results from production of an altered penicillin-binding protein (PBP2a) – Usually a healthcare-associated infection, elderly also higher risk colonisation vs infection – Can also be resistant to other antimicrobial classes – In hospital: isolate / cohort with contact precautions  S. aureus: Pathogenesis Portal of entry: Attaches to cells: 1. Surface proteins 1. Ingestion – Facilitate attachment 2. Penetration 2. Capsule a) A break in the skin – Inhibits chemotaxis, phagocytosis b) Entry through the – Facilitates adherence to implants mucous membranes 3. Fibrin/fibrinogen binding protein allowing access to (clumping factor) adjoining tissues – Attachment to blood clots & traumatised tissue 4. Matrix-binding proteins – Ex. adhesin – promotes collagen attachment – found in strains that cause osteomyelitis or septic arthritis  S. aureus: pathogenesis Defeating/ evading the immune system: Inhibition of phagocytosis with survival within phagocytes Production of extracellular substances that promote invasion – Invasins – Enzymes S. aureus: pathogenesis  S. aureus: pathogenesis Damage to host cells: Gets out & spreads further: Direct damage – peptidoglycan Person-to-person wall – direct contact via skin Enzymes (see previous slides) carriage, especially hands Toxins Environment – EXOtoxins: Superantigens – shed on to surfaces Toxic shock syndrome toxin (TSST-1) Enterotoxins – 8 antigenic types (A-E, G-I) – Cause food poisoning (will be covered in GIHEP module) – Exfoliative toxins Scalded skin syndrome – Other Cytotoxins (alpha, beta, leukocidin, etc)  CLASSIFICATION OF STAPHYLOCOCCAL INFECTIONS 1. Skin & soft tissue Spectrum of S. aureus Discussed briefly here, please infections also see the lecture ‘Skin and Soft Tissue Infections’ 2. Systemic – invasive 3. Toxin-mediated a) Food Poisoning / Gastroenteritis a) Short incubation period, self-limiting b) Covered in GIHEP module b) Scalded Skin Syndrome c) Toxic Shock Syndrome 2. SYSTEMIC S. AUREUS INFECTIONS Bloodstream infection (BSI) Endocarditis – Usually secondary to BSI – Will be covered in more detail in cardiovascular module Bone/joint infections – Ex. septic arthritis, osteomyelitis – Please see lecture on bone & joint infections for more detail Deep abscesses, e.g. brain, spine, psoas muscle Pneumonia – Risk factors: viral respiratory infection, cystic fibrosis, ventilation, aspiration – Will be discussed further in respiratory module  3. Toxin-mediated: Scalded Skin Syndrome Spectrum of superficial blistering skin disorders – Localized blisters – Generalized exfoliation of entire body surface – Mucous membranes usually spared Exfoliative toxins – Toxins spread haematogenously from a localised source – Split intracellular bridges in skin layer (middle layers) Most common in children < 6 yrs – Mainly in neonates – Immunosuppressed adults / renal failure Contagious ++ Mortality: Children